POS0779 BRAIN TUMOR-LIKE LESIONS AS FORM OF PRESENTATION OF NEUROPSYCHIATRIC LUPUS
Authors: I. L. Mamani Velarde, I. Altabás González, C. Mouriño Rodríguez, S. García Pérez, I. Hernández, J. M. Pego-Reigosa
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Neuropsychiatric (NP) systemic lupus erythematosus (SLE) encompasses a broad spectrum of syndromes.<sup>[1]</sup> The attribution of the NP manifestations to the disease itself is a challenge and is critical to select the correct treatment. <sup>[2]</sup> <h3>Objectives</h3> To present a case of a woman with SLE who developed brain tumor-like lesions. <h3>Methods</h3> The clinical manifestations, complementary tests, treatment are described. <h3>Results</h3> 28-year-old woman with a history of SLE with moderate disease (constitutional, cutaneous, musculoskeletal, hematologic and serological) and frequent flares despite treatment with hydroxychloroquine and doses of prednisone up to 20mg/day. She was admitted to the rheumatology service due to a severe flare-up of SLE, with headache, fever, worsening of lesions in photo-exposed areas, lymphadenopathy, arthralgia, nausea, and vomiting. Blood tests showed platelets 60,000/μL, elevated ESR, abnormal liver biochemical, decreased C3, normal urine, with no data of infectious etiology. After treatment with iv methylprednisolone (250mg x 3) and iv belimumab (600mg), she presented clinical and analytical improvement and was discharged from the hospital. Three days later, the patient presented persistent headache and fever, and decreased level of consciousness; laboratory tests showed leukocytosis, anemia, abnormal liver function tests, elevated ESR and CRP. She was referred to the emergency room. On the neurological exam: patient disoriented in time and space, opened her eyes only after painful stimulus, signs of dysarthria, and facial paralysis. CT scan revealed a space-occupying lesion (3 x 2cm), at the level of the right basal nuclei with perilesional edema and collapse of the anterior horn of the right lateral ventricle, discreet mass effect with displacement midline, and similar contralateral involvement. The patient was admitted to the hospital due to a probable primary neoplasm of the central nervous system, without being able to initially exclude infectious, vascular, and inflammatory pathologies. Treatment was started with iv dexamethasone and empiric therapy for bacteria, viruses, fungi, and parasites. The following day, brain MRI (Figure 1, A - B) showed lesions in the right and left basal ganglia, with a mass effect in the right basal ganglia and images of their interior with artifact related to hemosiderin or deoxyhemoglobin, related to history of bleeding from the lesions. Alteration of thickness and irregular subependymal signal in the occipital horns. The stereotaxic brain biopsy showed parenchyma with intense acute inflammatory changes, with necrosis and vascular inflammation, without histopathological features of etiological specificity, and no evidence of neoplasia. The lumbar puncture did not show alterations, cytology without malignant cells, antibodies against onconeuronal proteins negative. Ruled out infectious etiology. Slow progressive improvement in clinical and laboratory manifestations and in imaging tests improvement was seen in response to the therapy with high doses of glucocorticoids and cyclophosphamide pulses. After prolonged hospitalization, she was discharged from the hospital, her neurological status being normal. Brain MRI (Figure 1, C-D), two months after discharge, showed a clear decrease in the size of the brain lesions. <h3>Conclusion</h3> To the best of our knowledge, no brain space-occupying lesions (simulating neoplasms) attributed to SLE have been described. The context of concomitant activity, the negative results for infectious/malignant diseases, and the favorable response to immunosuppressive treatment, support the neuroinflammatory etiology. <h3>References</h3> [1]Ainiala H, Hietaharju A, Loukkola J, et al. Validity of the new American College of Rheumatology criteria for neuropsychiatric lupus syndromes: a population-based evaluation. Arthritis Rheum. 2001;45(5):419-423. [2]Bortoluzzi A, Scirè CA, Govoni M. Attribution of Neuropsychiatric Manifestations to Systemic Lupus Erythematosus. Front Med (Lausanne). 2018 Mar 14; 5:68. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.